Purpose: Senior nursing and medical interns’ lack of familiarity and confidence with respect to practicing universal precaution for the prevention of occupational needlestick or sharp injuries may harm themselves. Trainees’ self-reported needlestick or sharp injury rate was known to be especially high during the first 2 months of internship in Taiwan. This prospective cohort study aimed to assess the effect of newly developed virtual reality (VR) game, which uses Gagne’s learning model to improve universal precaution for needlestick or sharp injury prevention and decrease the rates of needle stick or sharp injuries in new-coming medical and nursing interns in Taiwan.Methods: From 2017 to 2019, the VR system was developed and applied in training of 59 new-coming nursing and 50 medical interns. Occupational needlestick or sharp injury prevention was sought to be achieved through a game of right and wrong choices for safe or unsafe universal precaution behaviors.Results: In comparison with medical interns, a higher proportion of nursing interns had past experiences of deep occupational needlestick or sharp injury. Before VR training, the familiarity and confidence for needlestick or sharp injury prevention were higher among nursing interns than medical interns. Trainees with past experiences of deep needlestick or sharp injury exhibited better performance on the accuracy rate and time needed to complete 20 decisions than those without past experiences in VR practice. All trainees showed an improved performance after VR training. A high proportion of trainees reported that the VR-based training significantly decreased their anxiety about needlestick or sharp injury prevention.Conclusion: This self-developed VR game system using Gagne’s flow improved universal precaution for needlestick or sharp injury prevention and reduced the needlestick or sharp injury rates in the first 2 months of nursing and medical internship.

In obesity, there are no effective therapies for parallel immune and metabolic abnormalities, including systemic/tissue insulin-resistance/inflammation, adiposity and hepatic steatosis. Caffeine has anti-inflammation, antihepatic steatosis, and anti-insulin resistance effects. In this study, we evaluated the effects and molecular mechanisms of 6 wk of caffeine treatment (HFD-caf) on immunological and metabolic abnormalities of high-fat diet (HFD)-induced obese rats. Compared with HFD vehicle (HFD-V) rats, in HFD-caf rats the suppressed circulating immune cell inflammatory [TNFα, MCP-1, IL-6, intercellular adhesion molecule 1 (ICAM-1), and nitrite] profiles were accompanied by decreased liver, white adipose tissue (WAT), and muscle macrophages and their intracellular cytokine levels. Metabolically, the increase in metabolic rates reduced lipid accumulation in various tissues, resulting in reduced adiposity, lower fat mass, decreased body weight, amelioration of hepatic steatosis, and improved systemic/muscle insulin resistance. Further mechanistic approaches revealed an upregulation of tissue lipogenic [(SREBP1c, fatty acid synthase, acetyl-CoA carboxylase)/insulin-sensitizing (GLUT4 and p-IRS1)] markers in HFD-caf rats. Significantly, ex vivo experiments revealed that the cytokine release by the cocultured peripheral blood mononuclear cell (monocyte) and WAT (adipocyte), which are known to stimulate macrophage migration and hepatocyte lipogenesis, were lower in HFD-V groups than HFD-caf groups. Caffeine treatment simultaneously ameliorates immune and metabolic pathogenic signals present in tissue to normalize immunolgical and metabolic abnormalities found in HFD-induced obese rats.

Identification of new pharmacological approaches to inhibit the excessive fat intake-induced steatohepatitis and chronic kidney disease (CKD) is important. High-fat diet (HFD)-induced steatohepatitis and CKD share common pathogenesis involving peroxisome proliferator-activated receptor (PPAR)-α and -δ. Elafibranor, a dual PPARα/δ agonist, can ameliorate the HFD-induced steatohepatitis. Nonetheless, the effects of HFD-induced CKD had not yet explored. This study investigated the effects of elafibranor (elaf) on the progression of HFD-induced CKD in mice. In vivo and in vitro renal effects were evaluated in HFD-elaf mice receiving 12 weeks of elafibranor (from 13th to 24th week of HFD feeding) treatment. In elafibranor-treated HFD mice, increased insulin sensitivity, reduced obesity and body fat mass, decreased severity of steatohepatitis, increased renal expression of PPARα, PPARδ, SIRT1, and autophagy (Beclin-1 and LC3-II) as well as glomerular/renal tubular barrier markers [synaptopodin (podocyte marker), zona occludin-1, and cubulin], reduced renal oxidative stress and caspase-3, and less urinary 8-isoprostanes excretion were observed. Aforementioned benefits of elafibranor were associated with low renal tubular injury and tubulointerstitial fibrosis scores, less albuminuria, low urinary albumin-to-creatinine ratio, and preserved glomerular filtration rate. Acute incubation of podocytes and HK-2 cells with elafibranor or recombinant SIRT1 reversed the HFD-sera-induced oxidative stress, autophagy dysfunction, cell apoptosis, barrier marker loss, albumin endocytosis, and reuptake reduction. Besides hepatoprotective and metabolic beneficial effects, current study showed that elafibranor inhibited the progression of HFD-induced CKD through activation of renal PPARα, PPARδ, SIRT1, autophagy, reduction of oxidative stress, and apoptosis in mice with steatohepatitis.

Objectives: Inter-professional education (IPE) builds inter-professional collaboration (IPC) attitude/skills of health professionals. This interventional IPE programme evaluates whether benchmarking sharing can successfully cultivate seed instructors responsible for improving their team members’ IPC attitudes. Design: Prospective, pre-post comparative cross-sectional pilot study. Setting/participants: Thirty four physicians, 30 nurses and 24 pharmacists, who volunteered to be trained as seed instructors participated in 3.5-hour preparation and 3.5-hour simulation courses. Then, participants (n=88) drew lots to decide 44 presenters, half of each profession, who needed to prepare IPC benchmarking and formed Group 1. The remaining participants formed Group 2 (regular). Facilitators rated the Group 1 participants’ degree of appropriate transfer and sustainable practice of the learnt IPC skills in the workplace according to successful IPC examples in their benchmarking sharing. Results: For the three professions, improvement in IPC attitude was identified by sequential increase in the post-course (second month, T ₂ ) and end-of-study (third month, T ₃ ) Interdisciplinary Education Perception Scale (IEPS) and Attitudes Towards Healthcare Teams Scale (ATHCTS) scores, compared with pre-course (first month, T ₁ ) scores. By IEPS and ATHCTS-based assessment, the degree of sequential improvements in IPC attitude was found to be higher among nurses and pharmacists than in physicians. In benchmarking sharing, the facilitators’ agreement about the degree of participants’appropriate transfer and sustainable practice learnt ‘communication and teamwork’ skills in the workplace were significantly higher among pharmacists and nurses than among physicians. The post-intervention random sampling survey (sixth month, T _post ) found that the IPC attitude of the three professions improved after on-site IPC skill promotion by new programme-trained seed instructors within teams. Conclusions: Addition of benchmark sharing to a diamond-based IPE simulation programme enhances participants’ IPC attitudes, self-reflection, workplace transfer and practice of the learnt skills. Furthermore, IPC promotion within teams by newly trained seed instructors improved the IPC attitudes across all three professions.

Bacterial translocation (BT) and splenomegaly contribute to cirrhosis-associated immune dysfunction (CAID) including T cell depletion, infection, and chronic inflammation. β-blockers have been reported to decrease BT and improve splenomegaly. This study explores the modulation of β1 and β2 adrenergic receptors (ADRB1/ADRB2) by propranolol treatment on the peripheral and splenic immune dysfunction of cirrhotic mice. In vivo experiments were performed in bile duct ligation (BDL)- and thioacetamide (TAA)-cirrhotic mice receiving two weeks of propranolol treatment. Acute effects of propranolol were evaluated in T-helper (Th) cells isolated from spleen of cirrhotic mice. Over-expression of β1 and β2 adrenergic receptors (ADRB1/ADRB2) in spleen and T lymphocytes was associated with high peripheral/splenic lipopolysaccharide binding protein levels. Moreover, a decrease in Th cells percentage, increase in Treg subset, and cytokines were accompanied by increased apoptosis, proliferation, and reduced white pulp hyperplasia in cirrhotic mice, which were counteracted by propranolol treatment. The Th-cell depletion, systemic inflammation, BT, and infection were improved by chronic propranolol treatment. Acute propranolol treatment inhibited apoptosis, Treg-conditioned differentiation, and promoted Th2-conditioned differentiation through ADRB-cyclic adenosine monophosphate (cAMP) signals in cirrhotic mice. In conclusion, suppression of ADRB1 and ADRB2 expressions in spleen and splenic T lymphocytes by acute and chronic propranolol treatment ameliorate systemic and splenic immune dysfunction in cirrhosis.

Background: Reversal of alcohol-induced peroxisome proliferator-activated receptor (PPAR) α (PPARα) and PPARδ dysfunction has been reported to decrease the severity of alcoholic steatohepatitis (ASH). Autophagy is essential for cell survival and tissue energy homeostasis. Emerging evidence indicates that alcohol-induced adipose tissue (AT) autophagy dysfunction contributes to injury in the intestine, liver, and AT of ASH. Methods: The effects and mechanisms of dual PPARα/δ agonist elafibranor on autophagy stimulation were investigated using mice with ASH. Results: C57BL/6 mice on ethanol diet showed AT dysfunction, disrupted intestinal barrier, and ASH, which was accompanied by alcohol-mediated decrease in PPARα, PPARδ, and autophagy levels in intestine, liver, and AT. Chronic treatment with elafibranor attenuated AT apoptosis and inflammation by restoration of tissue PPARα, PPARδ, and autophagy levels. In ASH mice, alcohol-induced AT dysfunction along with increased fatty acid (FA) uptake and decreased free FA (FFA) release from AT was inhibited by elafibranor. The improvement of AT autophagy dysfunction by elafibranor alleviated inflammation and apoptosis-mediated intestinal epithelial disruption in ASH mice. Acute elafibranor incubation inhibited ethanol-induced ASH-mice-sera-enhanced autophagy dysfunction, apoptosis, barrier disruption, and intracellular steatosis in Caco-2 cells and primary hepatocytes (PHs). Conclusion: Altogether, these findings demonstrated that the PPARα/δ agonist, elafibranor, decreased the severity of liver injury by restoration of alcohol-suppressed AT autophagy function and by decreasing the release of apoptotic markers, inflammatory cytokines, and FFA, thereby reducing intestinal epithelium disruption and liver inflammation/apoptosis/steatosis in ASH mice. These data suggest that dual PPAR agonists can serve as potential therapeutic agents for the management of ASH.